Mechanism of lipid peroxide formation in polychlorinated biphenyls (PCB) and dichlorodiphenyltrichloroethane (DDT)-poisoned rats.

To clarify the mechanism of lipid peroxide formation in polychlorinated biphenyls (PCB)-poisoned rats, the following two experiments were carried out. Experiment No. 1: Rats were separated into three groups. Group 1 was fed a normal diet, group 2 was fed a PCB-supplemented diet, and group 3 was fed a dichlorodiphenyltrichloroethane (DDT)-supplemented diet. After 5 months, the rats were killed. The thiobarbituric acid (TBA) values in livers of the PCB- and DDT-exposed rats had increased. The activity of catalase was increased in the PCB-fed rats but decreased after the administered of DDT. The glutathione peroxidase activity was decreased only in the PCB-administered rats. These results indicate that PCB and DDT have some effects to enhance lipid oxidation. It is probable that the decrease in glutathione peroxidase is the major reason for the increase of lipid oxidation in PCB-poisoned rats. The mechanism of lipid peroxidate production in DDT-poisoned rats could be different from the case of PCB poisoning. Experiment No. 2: Rats were separated into two groups. To one group, normal diet was given and to the other group PCB-supplemented diet was given. After 1 month, the rats were killed. In PCB-exposed rats, activities of glutathione reductase and glutathione S-transferase were increased. The increase in glutathione reductase and glutathione S-transferase were increased. The increase in glutathione reductase could be a compensation for a decrease in glutathione peroxidase. It is probable that PCB is metabolized to make glutathione conjugates by the action of glutathione S-transferase.